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EDITOR—Sithamparanathan makes valid points about problems with handovers.1 During the past three months a formal handover process has been instituted at this hospital. The bed manager, site coordinator, and clinical support workers are present at the handover. …

A few years ago, I had just obtained my first job at specialist registrar level and was posted to a new hospital. Having only limited endoscopy skills, I was naturally apprehensive about the responsibilities of the new job and the expectations of being a specialist registrar. After the morning induction period, I was suddenly told that I was due on the endoscopy unit that afternoon and was expected to do my own list as the previous registrar had done over the past year. …

Junior doctors are frequently changing jobs and have to get used to new working environments. Here, I provide some useful tips that are not usually given on the induction day.

Several years ago I had just obtained my MRCP and was feeling on top of the world. A short term post for second on call became available at my hospital, and I was deemed capable of filling it. As it was my first such job, I asked for some advice from the other registrars on the unit. A common theme among them was to be wary of inpatient medical referrals from the …

Registrars and some senior house officers will find themselves having to lead an on-call team. This can be quite daunting and takes time to adjust to. Here are some tips.

When preregistration house officers move to senior house officer grade they are expected to attend outpatient clinic sessions. Here are some tips on how to make sure your clinic sessions run smoothly.

Editor—We appreciated the report by O'Beirne and Cairns concerning a patient with liver test dysfunction in the setting of treatment with the COX 2 inhibitor celecoxib.1 We are, however, concerned at their use of “cholestatic hepatitis” as the most appropriate description of the pattern of liver test abnormality observed. The patient they described had a maximal aspartate transaminase concentration of 1650 IU/l (reference range 10-40 IU/l), a maximal alkaline phosphatase concentration of 232 IU/l (25-115 IU/l), and peak total serum bilirubin of 123 μmol/l (5-20 μmol/l). In broad terms, two categories of drug associated liver injury are encountered commonly, namely cholestatic and hepatocellular.2 Cholestatic injury has been defined further as occurring when the peak transaminase concentration is less than eight times the upper limit of normal, and the corresponding ALP is greater than threefold normal, whereas hepatocellular injury has been defined as being present when the peak transaminase concentration is greater than eight times the upper limit of normal and the concomitant alkaline phosphatase concentration is less than threefold normal. A mixed pattern of injury, showing features of both, may also be found.3 According to these criteria the patient of O'Beirne and Cairns had evidence of hepatocellular injury primarily, rather than a mixed pattern as the term “cholestatic hepatitis” suggests. Liver biopsy might have helped to emphasise this distinction. The article by Maddrey et al referred to in their report was misquoted4: where the term alkaline phosphatase was used, it should have read alanine aminotransferase. In that study only 0.4% and 0.3% respectively of 6376 patients treated with celecoxib had maximal alanine aminotransferase and aspartate transaminase concentrations greater than or equal to three times the upper limit of normal. None of these transaminase elevations was greater than eight times the upper limit of normal, in contrast to that found in the patient of O'Beirne and Cairns (about 41 times upper normal limit). Therefore, although we disagree with the view that this patient had cholestatic hepatitis on the basis of data quoted, the case does represent the first reported instance of severe hepatocellular liver dysfunction in association with celecoxib treatment.